An ideal treatment for the inactivation of viruses which contaminate transfusable blood products would specifically interact with viral nucleic acid, thereby eliminating damage to platelets and red blood cells which are anucleate. In our initial studies on the photoinactivation of viruses we demonstrated that low intensity laser-UV radiation at 308nm (UVB) reduced poliovirus activity by 4-6 log10 at doses (fluences) which did not disrupt platelet aggregation activity or induce the release of platelet serotonin. High intensity laser-UV did not increase viral killing, but caused damage to platelet and plasma proteins. Exogenously added albumin protected both platelets and virus from UVB damage at the high laser intensities. We are currently examining the antiviral activity of the photoactivatable compound gilvocarcin (GV), an antitumor agent which is closely related to psoralen. GV binds to DNA in the presence of near UV radiation (UVA) through cycloaddition, blocks DNA replication, and causes strand breaks. We have demonstrated photoinduced damage of DNA on agarose gels following treatment of plasmid pBR322 with GV (100 ng/mL) and laser UVA (350nm). Preliminary work with GV (to lOOng/mL) demonstrated no effect on the viability of the marker viruses, bacteriophages PM2 or T2, using either of 2 light sources (UVA germicidal lamp at 365nm and UV laser at 350nm). Similar studies are underway with four additional bacteriophages: 06 (ds RNA, lipid envelope), PRD1 (ds DNA, internal lipid), 0X174 (ss DNA, no lipid) and T7 (ds DNA, no lipid). The concentration of GV has been increased to 1 ug/ml and a UVA source with peak output at 365nm is being used to achieve a maximum radiation exposure of 0.42 J/cm. The sensitivity of cells to gilvocarcin and radiation will be examined with monkey kidney cells (ability to support HSV infection) and mouse lymphoma cells (L5178Y, colony formation). Results of the UVB study were published in Blood 70:589 (FY'87).